Disorders of Small Intestine / Colon Flashcards

1
Q

Malabsorptive Disorders of the Small Intestine

A

Celiac Disease
Whipple Disease
Bacterial Overgrowth
Short Bowel Syndrome
Lactose Intolerance

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2
Q

Normal digestion is broken down into 3 phases

A
  1. Intraluminal: dietary fats, proteins, carbs are hydrolyzed and solubilized by pancreatic and biliary secretions
    - Fats are broken down by pancreatic lipase to monoglycerides and fatty acids that form micelles with bile salts
    - Micelles are important for solubilization and absorption of fat-soluble vitamins (A, D, E, K)
    - Proteins are hydrolyzed by pancreatic proteases to di and tripeptides and amino acids
  2. Mucosal: requires sufficient surface area of intact small intestinal epithelium
    - Brush border enzymesare important in the hydrolysis of disaccharides and di-and tripeptides
    - Malabsorption of specific nutrients may occur as a result of a deficiency in an isolated brush border enzyme
  3. Absorptive
    - Impaired absorption of chylomicrons and lipoproteins may lead to steatorrhea and significant enteric protein losses
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3
Q

which malabsorptive disorder has an abnormal response to gluten/gliadin?

A

Celiac Disease

Permanent dietary disorder caused by an immunologic response to gluten, which is a storage protein found in certain grains
Results in diffuse damage to the proximal small intestinal mucosa with malabsorption of nutrients

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4
Q

celiac dz is MC in who?

A
  1. M/C - Caucasians
  2. Genetic predisposition
    - First and second degree relatives are at higher risk
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5
Q

pathophys of celiac dz

A
  1. Dietary gluten triggers immune response that damages proximal small
    Intestine mucosa and cause villous atrophy
  2. Results in malabsorption of nutrients
  3. Wheat-containing foods, cause gluten and gliadin build up in intestinal mucosa, causing direct damage
  4. Also causing humoral immune and slight T-Cell mediated response causing antibody
    production
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6
Q

classic presentation of celiac dz

A
  1. Diarrhea, Steatorrhea, Flatulence - Bulky, foul-smelling, floating
  2. Dyspepsia
  3. Weight loss
  4. Abdominal distention
  5. Weakness, Muscle Wasting
  6. Growth Retardation in Children
  7. Resolution of sx upon Gluten-containing food withdrawal
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7
Q

atypical presentation of celiac dz

A

Fatigue, Depression
Iron-Deficiency Anemia, Vitamin B12 or Folate deficiency
Osteoporosis, bone pain
Amenorrhea, Infertility
Easy Bruising
Peripheral neuropathy, Ataxia
Dermatitis herpetiformis
Delayed puberty
Increased risk for gastric cancer

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8
Q

Pruritic papulovesicular rash - itchy
Extensor surfaces of extremities and trunk, scalp, and neck
Most pt have Celiac Disease

what are these lesions

A

Dermatitis Herpetiformis

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9
Q

diagnostic work-up for celiac disease

A
  1. IgA TTG antibody tests - 98% sens/specificity
  2. Total IgA levels
  3. IgA anti-endomysial antibody and IgG DGP (deamidated gliadin peptides)
    gliadin - protein found in wheat gluten
  4. Levels become undetectable after 6-12 months of gluten free diet
    - Used to monitor progress/compliance
  5. any vitamin/nutrient deficiencies

Pt continues to eat normally before testing

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10
Q

what enzyme is released by inflammatory cells that change the chemical structure of gliadin, making gliadin more immunogenic

A

tissue transglutaminase (TTG)

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11
Q

IgA TTG falsely negative in patients with ?

A

IgA deficiency

hence why get total IgA levels for celiac dz

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12
Q

imaging for celiac dz

A
  1. Endoscopic mucosal bx of proximal and distal duodenum - dx
    - mucosal bx for negative serum but have sx too
  2. Atrophy of duodenal folds shown on endoscopy
    - Or nodular, scalloping of duodenal folds, fissuring, & mosaic patterns of duodenal mucosa
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13
Q

Histology in endoscopic mucosal bx shows intraepithelial lymphocytosis
Blunting or a complete loss of intestinal villi

what is this dx

A

celiac dz

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14
Q

management for celiac dz

A
  1. avoid gluten 4eva - wheat, rye, barley
  • Improvement w/n 1-2 wks
  • Dietary supplements if vitamin deficient
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15
Q

cause of whipple dz

A

Tropheryma whipplei - G+, non-acid fast, PAS positive bacillus; ubiquitous in environment

Rare malabsorptive infectious disease

  • fecal-oral tramission
  • easily spreads throughout body = evades immune response
  • immunodeficiency is predisposing factor (hypothesis)
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16
Q

presentation of whipple disease

A
  1. Continually changing sx
  2. MC sx:
    - Arthralgias - 1st sx noted
    - Diarrhea, abd pain
    - wt loss (MC)
  3. other GI: malabsorption, gas, steatorrhea
  4. neurological possible: dementia, lethargy, coma, seizures
  5. PE: Low-grade F, malabsorption signs, enlarged joints, LAN
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17
Q

work-up + result for whipple dz

A
  1. DX: upper endoscopy w/ bx of duodenum - Macrophages w/ G+ bacilli (PAS positive macrophages) (pathognomonic)
  2. Confirm: PCR - done only if endoscopy is inconclusive
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18
Q

tx for whipple dz

A
  1. IV Ceftriaxone x 2-4 wks
    - allergic: IV Meropenem x 2-4 weeks
  2. Then TMP-SMX BID x 1 yr
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19
Q

A condition in which colonic bacteria are seen in excess in the small intestines; when present, intestinal symptoms can arise

A

Small Intestine Bacterial Overgrowth

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20
Q

Stomach and proximal short bowel contains only a small amount of bacteria d/t ?

A

gastric acidity and effects of peristalsis

An intact ileocecal valve helps prevent retrograde translocation of bacteria

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21
Q

causes of Small Intestine Bacterial Overgrowth

A
  1. Motility disorders
  2. Anatomic disorders (adhesions from prior surgeries)
  3. Other metabolic disorders (DM)
  4. Immune disorders
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22
Q

sx of Small Intestine Bacterial Overgrowth (SIBO)

A
  1. Some asx until vitamin def
  2. bloating, flatulence, diarrhea/steatorrhea, wt loss, acne, rashes

SIBO suspected with aforementioned sx and a hx of GI surgery or predisposed

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23
Q

work-up for SIBO

A
  1. confirm: small intestine aspiration w/ cx - invasive tho
  2. carbohydrate breath test - administration of lactulose = early peak in breath hydrogen lvls
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24
Q

how does a carbohydrate breath test work for SIBO?

A

metabolism of a test dose of carbohydrate substrate (lactulose, glucose) by bacterial flora leads to production of hydrogen, which is absorbed and ultimately excreted in the breath

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25
Q

how to prep for a carbohydrate breath test?

A

one day before test:

  1. Stop using all meds related to your GI tract (acid suppression, abd pain/spasm, D/C)
  2. NO carbs in following categories: bread, pasta, potatoes, rice, crackers, oatmeal, cereals, or any other starchy food products.
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26
Q

tx for SIBO

A
  1. When possible, anatomic defect corrected
  2. 7-10 d abx
    - Ciprofloxacin 500mg BID preferred
    - Augmentin
    - TMP-SMX
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27
Q

cause of short bowel syndrome

A
  1. Secondary to removal of portion of small intestine
  2. d/t Crohn’s dz, ischemia, tumor, trauma, mesenteric infarction, volvulus
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28
Q

sx of short bowel syndrome

A

Vary depending on amount and section of intestine removed

  1. Terminal ileal resection = malabsorption of B-12 and bile salts
  2. Extensive bowel resection
    - >50% of total length of small intestine
    - wt loss and diarrhea d/t nutrient malabsorption
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29
Q

management for acute phase of short bowel syndrome

A

Initial 3-4 wks after resection

  1. Stabilize large fluid/lyte losses
  2. Acid suppression - IV PPI
  3. Parenteral nutrition, graduating to enteral feeding
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30
Q

Management of Adaptation phase in short bowel syndrome

A
  1. Transition to oral feedings in slow and stepwise manner over a period of wks-months
  2. Complex carbohydrates
  3. Low fat
  4. Fluid management
  5. PPIs
  6. Antidiarrheals prn
  7. abx for SIBO
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31
Q

a brush border enzyme that hydrolyzes the disaccharide lactose into glucose and galactose

A

lactase

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32
Q

cause of lactase deficiency

A

deficiency of lactase

  • lactase steadily declines with age
  • MC non-European descendants
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33
Q

presentation of lactose intolerance

A

diarrhea, bloating, flatulence, and abdominal pain after ingestion of dairy products

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34
Q

work-up for lactose intolerance

A
  • DX: hydrogen breath test
  • After ingestion of 50g of lactose, a rise in breath hydrogen within 90 min is a positive test

Pt should be fasting for 8 hrs prior to test

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35
Q

tx for lactose intolerance

A
  • Lactose free diet/Lactose minimizing diet
  • Lactase supplementation - Lactaid
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36
Q

A condition in which there is neurogenic failure or loss of peristalsis in the intestine in the absence of any mechanical obstruction

what is this dx

A

Paralytic Ileus

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37
Q

Paralytic Ileus is MC in who?

A

in hospitalized pts as a result of:

  • Intra-abdominal processes such as recent GI or abdominal surgery
  • Peritoneal irritation (pancreatitis, hemorrhage)
  • Severe medical illness (pneumonia, sepsis, respiratory failure)
  • Meds that affect intestinal motility (opiods, anticholinergics)
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38
Q

Following surgery, which part of the digestive system usually normalizes first in motility?
followed by what part? (after 24-48 hours)
then what? (48-72 hours)

A

small intestinal motility first
stomach
colon

There is a “normal” period of time, lasting <4 d: from surgery until passage of flatus or stool and tolerance of an oral diet

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39
Q

cause/pathophys of paralytic ileus

A
  1. After abd surgery, it results from inflammatory response to intestinal manipulation and trauma
    - activates local macrophages = muscle dysfunction
  2. Inhibitory neural reflexes act locally through noxious spinal afferent signals that increase inhibitory sympathetic activity = Slowing motility
  3. Opioids inhibit GI tract motility = Increase resting tone while decreasing motility and emptying
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40
Q

presentation of paralytic ileus

A

N/V/obstipation, abdominal discomfort
Abdominal distention with tympany to percussion
Diminished/Absent bowel sounds
Diffuse abdominal pain

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41
Q

work-up for paralytic ileus

A

Can be clinical diagnosis if last >4 d

  1. Plain films - Distended/dilated gas-filled loops of bowel
    - Air in colon and rectum as well
  2. CT - if can’t distinguish ileus vs SBO
  3. labs:
    - CBC: r/o infection, ischemia, or abscess
    - CMP: hypokalemia can worsen ileus
    - BUN/Creatinine: uremia can lead to ileus
    - LFTs, Amylase, Lipase: gallbladder dysfunction or pancreatitis can lead to ileus
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42
Q

tx for paralytic ileus

A
  1. Underlying cause
  2. Complete Bowel rest
    - IV fluids/TPN
    - NG tube
  3. Slowly advance diet
  4. Activity
  5. Remove drugs that reduce intestinal motility
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43
Q

prevention of paralytic ileus

A
  1. avoid IV opioids
  2. Early ambulation, initiation of clear liquid diet
  3. Gum chewing - chewing stimulates vagus nerve = promotes peristalsis = release of normal GI tract hormones
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44
Q

pathophys of small bowel obstruction

A
  1. impairment in normal flow of intraluminal contents
  2. Mechanical obstruction - extrinsic/intrinsic obstacle prevents progression of intestinal contents
    - Simple/partial obstruction occludes lumen only
    - Full with strangulation impairs blood supply = necrosis of intestinal wall
    - Obstruction = progressive dilation of intestines proximal to blockage, while distal to the blockage the bowel will decompress
    - Activity of smooth muscle of small bowel increases in an attempt to propel contents past obstruction
    - Swallowed air/gas from bacterial fermentation can accumulate, adding to bowel distention
    - normal absorptive function lost, and fluid sequestered into bowel lumen and ongoing emesis = additional loss of fluids = hypovolemia
    - Bacterial overgrowth can also occur in proximal small bowel, which can cause emesis to become feculent
    - Excessive dilation = compressed intramural vessels of the small intestines
    — Reduced Perfusion to wall
    — tissue ischemia = necrosis and perforation
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45
Q

Most of SBO are a result of what

A

post-surgical adhesions

46
Q

s/s of SBO

A
  1. Acute presentation
  2. N/V
  3. Colicky abd pain
  4. Obstipation
  5. Other sx depend on area of obstruction
    - Proximal: profuse emesis containing undigested food, upper abd. discomfort
    - Distal: diffuse and poorly localized crampy abd pain; Feculent vomiting
  6. strangulation - fever, peritonitis
  7. dehydration (hallmark) - Tachycardia and hypotension
  8. abd distention -60% of pts
  9. High-pitched “tinkling” with auscultation
47
Q

upon auscultation of a pt suspected of SBO, you hear hyperactive bowel sounds, what does this indicate?

A

occur early as gastrointestinal (GI) contents attempt to overcome the
obstruction

hypoactive = happens later in disease process

48
Q

you’re worried about a pt has intestinal ischemia due to SBO, what are those signs?

A

fever
tachycardia
peritoneal signs - guarding, rigid abdomen, rebound tenderness, pain out of proportion to the examination

49
Q

work-up for SBO

A
  1. labs:
    - CBC, CMP
    - Lab findings reflect intravascular volume depletion d/t dehydration
    - Leukocytosis
    - prerenal failure (dehydration)
    - Electrolyte disorders
  2. imaging
    - DX: Plain xrays of abd
    - CT of abdomen and pelvis - visualize specific location and if bowel compromise
50
Q

xray of the abdomen shows
Dilated small bowel loops with air-fluid levels
Air fluid levels with a “ladder like” appearance

what is the dx?

A

SBO

51
Q

tx for SBO

A
  1. Admit and get surgical consult
    - Immediate surgery for bowel compromise (ischemia, perforation, necrosis)
  2. Vigorous fluid resuscitation and correct lytes
  3. GI decompression w/ NG tube
  4. Serial monitoring
  5. TPN
  6. abx only if bowel compromise (necrosis, perforation) - broad spectrum
52
Q

Spontaneous massive dilatation of the cecum and proximal colon in the absence of an anatomic lesion

A

Ogilvie Syndrome

53
Q

progressive dilation may result to what?

A

perforation

54
Q

ogilvie syndrome is MC in who?

A

Severely ill, hospitalized

  1. Postoperative (MC)
  2. Vent dependant
  3. Severe electrolyte abnormalities
55
Q

cause of ogilvie syndrome

A

precise mechanism unknown

associated with trauma, anesthesia, and pharmacological agents suggest impairment of ANS

56
Q

s/s of ogilvie syndrome

A
  1. pts on vent or are unable to report sx due to altered mental status.
  2. Severely distended abd
    - N/V
    - Typically without pain
    - first sign
  3. Abdominal tenderness with some degree of guarding or rebound tenderness; signs of peritonitis are absent unless perforation has occurred.
  4. Bowel sounds may be normal or decreased.
57
Q

work-up for ogilvie syndrome

A
  1. CBC
  2. CMP - (lyte abnormalities)
  3. Plain radiographs
    - Dilated colon - Cecum to splenic flexure
  4. CT
    - Can be used to establish dx
    - R/o other causes of obstruction
58
Q

tx for ogilvie syndrome

A
  1. Conservative tx is first step (80% success in 1-2 days)
    - no/minimal abd tenderness
    - no F, no leukocytosis, and a cecal diameter <12 cm.
  2. tx underlying illness
  3. Decompress colon
    - nasogastric tube and a rectal tube placed
    - ambulate/rolled and knee-chest position
    - DC drugs reducing intestinal motility (opioids, anticholinergics, CCB)
    - Enemas if large amounts of stool
  4. NPO, IV fluids
  5. Serial abdominal x-rays (q12 hrs)
  6. Neostigmine if severe
    - Inhibits destruction of acetylcholine
    - This facilitates transmission of impulses across myoneural junction
59
Q

Disorders of the Colon

A
  1. IBS
  2. Inflammatory Bowel Disorders
    - Ulcerative Colitis
    - Crohn Disease
  3. Pseudomembranous Colitis
  4. Diverticular Disease
  5. Polyps of the Colon
  6. Cancer of the Colon
  7. Rectal Disorders - Hemorrhoids, Anal Fissure, Rectal Prolapse
60
Q

cause/pathophys of IBS

A
  1. Idiopathic
  2. Chronic GI sx NOT EXPLAINED BY PRESENCE OF STRUCTURAL/BIOCHEMICAL ABNORMALITY
    - Abnormal motility
    - Visceral hypersensitivity
    - Enteric infection
    - Psychosocial
61
Q

IBS is MC in who?

A

Women
Initial onset - late teens, early 20s

10% of adults have sx compatible with IBS

62
Q

pathogenesis of IBS

A
  1. Abnormal motility
    - Abnormal myoelectrical and motor abnormalities identified in colon correlated with episodes of abd pain or emotional stress
  2. Visceral Hypersensitivity
    - Lower visceral pain threshold, reporting pain at lower volumes of gas.
  3. Intestinal inflammation
    - Dietary factors, meds, or infections may increase intestinal permeability, leading to intestinal inflammation
    - Small intestine bacterial overgrowth
  4. Psychosocial abnormalities
    - depression, anxiety, somatization
    - chronic stress
    - alter intestinal motility or modulate nerve pathways
63
Q

presentation of IBS

A
  1. Idiopathic entity characterized by abd. pain with altered bowel habits, continuous or Intermittent
  2. Present 1 day per week
    - Abd. pain with +2 of following: Related to defecation, Change in stool frequency, Change in stool form
  3. Crampy, Lower abd Pain - relieved with defecation
    - does not occur at PM (usually)
  4. Change in stool frequency/form, urgency
    - Diarrhea, Constipation, Mixed
  5. abd distention; bloating
  6. other somatic sx: dyspepsia, heartburn, fatigue/myalgias, anxiety

sx MUST Be Present for at Least 3 MONTHS

64
Q

classifications for IBS

A
  1. IBS with diarrhea
  2. IBS with constipation
  3. IBS with mixed constipation and diarrhea
  4. IBS that is not subtyped

Based on predominant stool habits

65
Q

Rome IV criteria for IBS?

A

recurrent abdominal pain, on average, at least 1 day per wk in the last 3 months, associated with 2 or more of the following criteria:

  1. Related to defecation
  2. Associated with a change in stool frequency
  3. Associated with a change in stool form (appearance)
66
Q

what type of sx are NOT associated with IBS?

A

Alarm sx:

  • Severe progressive pain
  • Pain associated with anorexia or wt loss
  • Severe constipation
  • Severe diarrhea
  • Hematochezia/Rectal bleeding
  • wt Loss
  • Fever
67
Q

work-up for IBS

A
  1. CBC, C-Reactive protein, Celiac, Stool Studies
    - IF NEGATIVE: no other testing recommended
  2. colonoscopy - if >50 or fail conservative tx
    - NOT FOR YOUNG PTS (-) alarm sx
68
Q

management for IBS

A
  1. Reassurance, Support, & Education
  2. Food Diary & Dietary Modification
    - Avoidance fatty foods, spicy foods
    - Alcohol, caffeine
    - Avoidance of gas producing foods (beans, onions, wheat germ, etc)
    - Low FODMAP Diet - fermentable, sugars, polyols)
    - Fiber supplementation
  3. Behavioral Therapy/Relaxation Techniques
  4. Physical activity
  5. pharm
    - antispasmodics - Dicyclomine, Hyoscyamine
    - Antidiarrheal - Loperamide (prophylactic)
    - Laxatives - Osmotic Laxatives = Polyethylene glycol, lactulose, miralax
    - Specific IBS Drugs - Linaclotide,
    Lubiprostone, Alosetron
    - Psychotropic Agents - TCA, SSRI
69
Q

IBS indications for antispasmodics?

A

Diarrhea predominant with pain and bloating

70
Q

SE of antispasmodics

A

Urinary retention
Constipation
Dry mouth
Tachycardia

71
Q

indications for Alosetron (Lotronex)

A

Severe Diarrhea predominant IBS - in WOMEN
Diarrhea >6 months

72
Q

MOA of Alosetron (Lotronex)

A
  • Inhibits serotonin from binding to 5HT3 receptors in the intestine
  • Too much serotonin can cause hypermotility of the GI tract
73
Q

which med has a BBW for
Severe Constipation
Ischemic Colitis

and pt must sign a consent prior to use

A

Alosetron (Lotronex)

74
Q

indications for Linaclotide (Linzess)

A

Constipation predominant IBS

75
Q

MOA of Linaclotide (Linzess)

A

Guanylate cyclase agonist - Stimulates intestinal fluid secretion and transit

76
Q

SE of Linaclotide (Linzess)

A

Diarrhea, Dehydration

$$ Expensive! $$

77
Q

which med has a BBW for pts <18 and has a risk of dehydration?

A

Linaclotide (Linzess)

78
Q

indications for Lubiprostone (Amitiza)

A

Constipation predominant IBS in WOMEN
Chronic constipation

79
Q

MOA of Lubiprostone (Amitiza)

A

Selective Chloride Activator - activates ClC-2 chloride channels, increasing intestinal fluid secretion and motility and reducing intestinal permeability

80
Q

SE and CI of Lubiprostone (Amitiza)

A
  1. CI - Diarrhea, GI obstruction
  2. SE N/D, Fatigue, Dizziness

$$ Expensive!! $$

81
Q

what specific TCAs are used for
IBS with predominant pain and bloating
Due to SE - better for IBS with diarrhea and not constipation

A

amitriptyline (Elavil)
nortriptyline (Pamelor)
imipramine (Tofranil)

82
Q

pt education for IBS

A
  1. keep food diary
  2. stop eating triggering foods
  3. more fiber
  4. exercise (20-60 mins, 3-5 d/wk)
83
Q

what type of abx associated colitis is
Found throughout hospitals in rooms and bathrooms
Easily transmitted by hospital personnel
Alcohol hand sanitizers will NOT kill bacteria

A

C diff

Hand washing and use of disposable gloves are helpful in reducing transmission

84
Q

pathophys of abx associated colitis

A
  • abx disrupt normal bowel flora = spores germinate and bacterium to flourish
  • MC ampicillin, clinda, 3rd-gen cephalos, fluoroquinolones
  • sx begin during or shortly after abx, or 8 wks
85
Q

presentation of abx associated colitis

A
  1. Mild-moderate
    - greenish, foul-smelling watery diarrhea 5–15 x per day, lower abd cramps, +/- blood or mucus
    - PE: normal; mild LLQ tenderness
    - Serum WBC >15k
  2. Severe disease (fulminant)
    - F; hemodynamic instability; abd distention, pain, and tenderness
    - profuse diarrhea (>30)
    - WBC >30k
86
Q

complications with abx associated colitis

A

Dehydration
Weight loss
Hemodynamic instability
Toxic megacolon

87
Q

work-up for abx associated coltiis

A
  1. (+) NAAT for C. difficile toxin gene or (+) stool test for C. difficile toxin(s)
  2. Stool studies
    - PCR assays (higher sensitivity 97%)
    - Rapid EIAs for C. diff toxins - 1 sample = 75 - 90% sensitive; 2 samples = 90 - 95% sensitive
  3. Stool cx
  4. Can do abd. Radiographs or abd. CT scans with severe or fulminant sx to look for colonic dilation or wall thickening
88
Q

tx for abx associated Colitis

A
  1. Strict contact precautions
  2. DC inciting Abx
  3. Mild-mod
    - Fidaxomicin/Vanc x 10 d
    — Recurrent rates lower with fidaxomicin
  4. Severe (WBC >15K)
    - Vanc + Metronidazole IV
89
Q

indications for surgical consult for CDI?

A
  1. hypotension +/- vasopressors
  2. F
  3. ileus or significant abd distention
  4. peritonitis or significant abd tenderness
  5. mental status change
  6. WBC >20K
  7. serum lactate >2.2 mmol/L
  8. end organ failure
  9. no improvement after 3-5 days w/ max therapy
90
Q

what is the procedure of choice for patients with colonic perforation, necrosis, or abdominal compartment syndrome?

A

total abdominal colectomy

diverting loop ileostomy/colonic lavage is an alternative that has been associated with decreased mortality in limited studies.

91
Q

tx for abx associated colitis relapse?

A
  1. First episode - second course of same regimen or prolonged vanco
  2. 2 relapses = 7-wk tapering regimen of vanc:
    - 125 mg orally 4x daily x 14 d;
    - BID x 7 d;
    - QD x 7 d;
    - every other day x 7 d;
    - and every 3rd day x 2 wks
92
Q

Reduction in blood flow to a level insufficient for delivery of oxygen and nutrients for cellular metabolism
Acute arterial occlusion (embolic, thrombotic), Venous thrombosis, Hypoperfusion causing nonocclusive

what is this dx?

A

ischemic colitis

93
Q

3 major arteries supply the colon

A
  1. superior mesenteric
  2. inferior mesenteric
  3. internal iliac
94
Q

Ischemic Colitis is MC in who?

A
  1. older pts
  2. Most have atherosclerotic disease
  3. Most occur spontaneously d/t transient episodes of non occlusive ischemia
    - After cardiopulmonary bypass
    - Aortoiliac surgery
    - Mainly d/t vasoconstriction of vessels
    - meds, illicit drugs (cocaine), extreme exercising
    - 5% after surgery of ileoaortic or AAA, MI, or Bypass Surgery
95
Q

In young patients, colonic ischemia develops

A

Vasculitis
Coagulation disorders
Estrogen therapy
Long distance running

96
Q

risk factors for intestinal ischemia

A

any condition that reduces perfusion to the intestine, or that predisposes to mesenteric arterial embolism, arterial thrombosis, venous thrombosis, or vasoconstriction.

97
Q

presentation of ischemic colitis

A
  1. Rapid onset of mild cramping abd pain - (more with chronic)
  2. Tenderness over affected bowel (mostly left side)
  3. Diarrhea with hematochezia
  4. urgent desire to defecate
  5. Mild to moderate amount of rectal bleeding or bloody diarrhea occurring within 24 hrs of onset of abd pain

classic clinical description for acute intestinal ischemia: abd pain out of proportion to the PE

98
Q

Patients with chronic mesenteric ischemia complain of recurrent abdominal pain after what?

A

eating

inability to increase blood flow to meet the demand of the intestine postprandially

99
Q

work-up for ischemic colitis

A
  1. labs: CBC, CMP, coag, increased LDH and CPK, stool studies
  2. first-line: CT w/ contrast of abdomen - edema and thickening of bowel wall in a segmental pattern
    “Target/thumbprinting/double halo”
  3. Colonoscopy diagnostic
    - Everyone suspected of ischemic colitis should receive
    - within 48 hours unless pt has evidence of irreversible damage on CT
    - Can detect mucosal lesions, bx, friable mucosa, erythema
100
Q

tx for ischemic colitis

A
  1. MC supportive care - Bowel rest: NPO; IV fluids; Observation
  2. Surgical intervention indicated clinical deterioration
    - Surgical resection of ischemic segment: Ongoing pain; Persistent fever; Leukocytosis; Peritoneal irritation; GI bleeding
  3. empiric abx
  4. Anticoagulant therapy - if mesenteric venous thrombosis
101
Q

complication with ischemic colitis

A

gangrene

102
Q

MC congenital abnormality of small bowel

A

Meckel’s Diverticulum

incidental find on testing
MC axs, if so, before age 10
“rule of 2s” - 2% of population; 2ft from ileocecal valve; sx 2% of pt

103
Q

presentation, dx, and management for meckel’s?

A
  • crampy abd pain, N/V, bleeding
  • “Meckel’s Scan”/Nuclear medicine scan: looks for ectopic gastric mucosa
  • Surgery

Can be Confused with appendicitis

104
Q

“Outpockets” from the colon
Result from increased intraluminal pressure

A

diverticular dz

MC Sigmoid/Left Colon
Incidence increases with age

Chronic constipation, Low Fiber Diet, Colonic musculature works to move hard stools, develops hypertrophy, thickens, gets rigid, and fibrotic

105
Q

3 forms of diverticular disease?

A

Uncomplicated Diverticulosis
Diverticulitis
Bleeding Diverticula

106
Q

presentation and management of Uncomplicated Diverticulosis

A

Asx MC; Screening labs normal

abd. pain, chronic constipation or fluctuating bowel habits possible
PE may be normal; mild LLQ tenderness, with palpable sigmoid and descending colon possible

Tx: high fiber diet

107
Q

presentation of Acute Diverticulitis

A
  1. Acute LLQ pain
    - Low grade Fever, Bowel changes, N/V, Blood in stool
  2. LLQ tenderness, palpable mass
  3. Leukocytosis mild to moderate
108
Q

work-up for Diverticular Disease

A
  1. MC: CT of abdomen
    - esp fever, leukocytosis, and signs of sepsis or peritonitis or with immunocompromise
    - Also obtained in those presenting for the first time with mild sx to look for evidence of diverticulitis
  2. colonoscopy for pts who respond to acute management
    - 4-8 wks after resolution
    - CI during d/t risk of free perforation
109
Q

tx for Diverticular Disease (uncomplicated)

A

conservative

  1. Mild sx and no peritoneal signs - clear liquid diet x 2-3 d
  2. Oral Ant
  3. abx (Esp immunocompromised)
    - Metronidazole + a quinolone
    - Metronidazole + TMP/SMX
    - Augmentin
  4. After resolution, high-fiber diet
110
Q

tx for Diverticular Disease (complicated)

A
  1. NPO with IV fluids
  2. pip-taz IV x 5-7 d, then switch to oral
    - Cipro + Metronidazole 10-14 d PO
  3. Surgery for SEVERE disease or do not improve after 72 hrs
111
Q

Criteria for inpatient treatment of Diverticulitis include:

A

CT shows complicated diverticulitis with perforation
Pt with sepsis
Immunosuppression
High fever ( > 102.5F/39C)
Severe abdominal pain
Age > 70
Significant comorbidities
Intolerance of oral intake
Failed outpatient treatment
Noncompliance, unreliability for return/follow-up

112
Q

MCC of lower GI bleed?

A

Diverticular Bleed

May resolve on own
Colonoscopy with cauterization of bleed